Matthias Jaeger

Continuous Monitoring of Cerebrovascular Autoregulation After Subarachnoid Hemorrhage by Brain Tissue Oxygen Pressure Reactivity and Its Relation to Delayed Cerebral Infarction

Background and Purpose— Disturbances of cerebrovascular autoregulation are thought to be involved in delayed cerebral ischemia and infarction after aneurysmal subarachnoid hemorrhage (SAH). We hypothesized that the continuous monitoring of brain tissue oxygen (PtiO2) pressure reactivity enables the detection of impaired autoregulation after SAH and that impaired autoregulation is associated with delayed infarction. Methods— In 67 patients after severe SAH, continuous monitoring of cerebral perfusion pressure (CPP) and PtiO2 was performed for an average of 7.4 days. For assessment of autoregulation, the index of PtiO2 pressure reactivity (ORx) was calculated as a moving correlation coefficient between values of CPP and PtiO2. Higher ORx values indicate disturbed autoregulation, whereas lower ORx values signify intact autoregulation. Results— Twenty patients developed delayed cerebral infarction, and 47 did not. Mean ORx was significantly higher in the infarction group compared with the noninfarction group (0.43±0.09 vs 0.23±0.14, respectively; P<0.0001). In a day-by-day analysis, ORx did not differ between groups from days 1 to 4 after SAH but was significantly higher from day 5 onward in the infarction group, indicating a deficit of autoregulatory capacity. In a logistic-regression model, ORx values from days 5 and 6 after SAH carried predictive value for the occurrence of delayed infarction but before this event ultimately occurred (P=0.003). Conclusions— ORx indicates impaired autoregulation in patients who develop delayed infarction after SAH. Furthermore, this index may distinguish between patients who finally develop delayed infarction and those who do not.

Continuous assessment of cerebrovascular autoregulation after traumatic brain injury using brain tissue oxygen pressure reactivity.

Objective:To evaluate whether two newly developed indexes of brain tissue oxygen pressure reactivity (ORx and bPtio2) provide information on the status of cerebrovascular autoregulation after traumatic brain injury. This was accomplished by analyzing the relationship between these indexes and an index of cerebrovascular pressure reactivity (PRx). PRx is an established parameter for estimation of cerebrovascular autoregulation. Design:Retrospective analysis of prospectively collected data. Setting:Neurosurgical intensive care unit of a university hospital. Patients:Twenty-seven patients suffering from severe traumatic brain injury. Interventions:Continuous monitoring of mean arterial blood pressure, intracranial pressure, cerebral perfusion pressure, and partial pressure of brain tissue oxygen (Ptio2) was performed for an average of 6.5 days. ORx was calculated as a moving correlation coefficient between values of cerebral perfusion pressure and Ptio2. The bPtio2 was calculated as a moving value of the slope of the linear regression function between cerebral perfusion pressure and Ptio2. PRx was calculated as a moving correlation coefficient between values for intracranial pressure and mean arterial blood pressure. Outcome was assessed at 6 months after traumatic brain injury (Glasgow Outcome Scale). Measurements and Main Results:Both ORx and bPtio2 correlated significantly with PRx (r = .55 for ORx, r = .52 for bPtio2, p < .01). PRx and ORx showed a significantly negative correlation to the monitored Ptio2 values (r = −.42 for PRx, r = −.41 for ORx, p < .05) and outcome (r = −.52 for PRx, r = −.62 for ORx, p < .01), whereas bPtio2 did not. Conclusions:ORx and, to a lesser extent, bPtio2 correlated with the autoregulatory marker PRx and provide additional information about the status of cerebrovascular autoregulation after traumatic brain injury. The data also suggested that patients with impaired autoregulation are at increased risk for secondary cerebral hypoxia.

Correlation of continuously monitored regional cerebral blood flow and brain tissue oxygen

SummaryBackground. The purpose of this study was to investigate the relationship between continuously monitored regional cerebral blood flow (CBF) and brain tissue oxygen (PtiO2).Methods. Continuous advanced multimodal neuromonitoring including monitoring of PtiO2 (Licox, GMS) and CBF (QFlow, Hemedex) was performed in eight patients after severe subarachnoid haemorrhage (n=5) and traumatic brain injury (n=3) for an average of 9.6 days. Parameters were measured using a flexible polarographic PtiO2-probe and a thermal diffusion CBF-microprobe.Findings. Regarding the whole monitoring period in all patients, the data indicated a significant correlation between CBF and PtiO2 (r=0.36). In 72% of 400 analysed intervals of 30 minutes duration with PtiO2 changes larger than 5 mmHg, a strong correlation between CBF and PtiO2 existed (r > 0.6). In 19% of intervals a still statistically significant correlation was observed (0.3 < r < 0.6). During the remaining 9% no correlation was found (r < 0.3). Regarding the clinical stability of the monitoring devices, the CBF monitoring system allowed monitoring of CBF in 64% of the time when PtiO2 monitoring was possible only. Phases of non-monitoring were mostly due to fever of the patient, when the system does not allow monitoring to avoid overheating of the cerebral tissue.Conclusions. This study suggests a correlation between CBF and PtiO2. The level of PtiO2 seems to be predominately determined by regional CBF, since changes in PtiO2 were correlated in 90% of episodes to simultaneous changes of CBF.

Effects of cerebrovascular pressure reactivity-guided optimization of cerebral perfusion pressure on brain tissue oxygenation after traumatic brain injury

Objective:To evaluate the concept of a cerebrovascular pressure reactivity-guided optimal cerebral perfusion pressure after traumatic brain injury by analyzing the relationship between optimal cerebral perfusion pressure and brain tissue oxygen. Design:Prospective observational cohort study. Setting:Neurosurgical intensive care unit of a university hospital. Patients:Thirty-eight patients after head injury. Interventions: Continuous computerized monitoring of mean arterial pressure, intracranial pressure, and brain tissue oxygen for 5.3 ± 2.6 days. The index of cerebrovascular pressure reactivity was calculated as a moving correlation coefficient between spontaneous low-frequency fluctuations of mean arterial pressure and intracranial pressure. Optimal cerebral perfusion pressure was defined as the cerebral perfusion pressure level with the lowest average index of cerebrovascular pressure reactivity. Measurements and Main Results:Optimal cerebral perfusion pressure could be identified in 32 of 38 patients. Median optimal cerebral perfusion pressure was between 70 and 75 mm Hg (range, 60–100 mm Hg). Below the level of optimal cerebral perfusion pressure, brain tissue oxygen decreased in parallel to cerebral perfusion pressure, whereas brain tissue oxygen reached a plateau above optimal cerebral perfusion pressure. Optimal cerebral perfusion pressure correlated significantly with the cerebral perfusion pressure level, where brain tissue oxygen reached its plateau (r = .79; p < .01). Average brain tissue oxygen at optimal cerebral perfusion pressure was 24.5 ± 6.0 mm Hg. Conclusions:This study supports the concept of cerebrovascular pressure reactivity-based individual optimal cerebral perfusion pressure. Driving cerebral perfusion pressure in excess of optimal cerebral perfusion pressure does not yield improvements in brain tissue oxygen after head injury and should be avoided, whereas cerebral perfusion pressure below optimal cerebral perfusion pressure may result in secondary cerebral ischemia.

Clinical Significance of Impaired Cerebrovascular Autoregulation After Severe Aneurysmal Subarachnoid Hemorrhage

Background and Purpose— The purpose of this study was to investigate the relationship between cerebrovascular autoregulation and outcome after aneurysmal subarachnoid hemorrhage. Methods— In a prospective observational study, 80 patients after severe subarachnoid hemorrhage were continuously monitored for cerebral perfusion pressure and partial pressure of brain tissue oxygen for an average of 7.9 days (range, 1.9–14.9 days). Autoregulation was assessed using the index of brain tissue oxygen pressure reactivity (ORx), a moving correlation coefficient between cerebral perfusion pressure and partial pressure of brain tissue oxygen. High ORx indicates impaired autoregulation; low ORx signifies intact autoregulation. Outcome was determined at 6 months and dichotomized into favorable (Glasgow Outcome Scale 4–5) and unfavorable outcome (Glasgow Outcome Scale 1–3). Results— Twenty-four patients had a favorable and 56 an unfavorable outcome. In a univariate analysis, there were significant differences in autoregulation (ORx 0.19±0.10 versus 0.37±0.11, P<0.001, for favorable versus unfavorable outcome, respectively), age (44.1±11.0 years versus 54.2±12.1 years, P=0.001), occurrence of delayed cerebral infarction (8% versus 46%, P<0.001), use of coiling (25% versus 54%, P=0.02), partial pressure of brain tissue oxygen (24.9±6.6 mm Hg versus 21.8±6.3 mm Hg, P=0.048), and Fisher grade (P=0.03). In a multivariate analysis, ORx (P<0.001) and age (P=0.003) retained an independent predictive value for outcome. ORx correlated with Glasgow Outcome Scale (r=−0.70, P<0.001). Conclusions— The status of cerebrovascular autoregulation might be an important pathophysiological factor in the disease process after subarachnoid hemorrhage, because impaired autoregulation was independently associated with an unfavorable outcome.

Monitoring of brain tissue oxygenation following severe subarachnoid hemorrhage.

Abstract The purpose of this prospective observational study was to investigate the relation between the frequency of critical neuromonitoring parameters (brain tissue pO2, (PtiO2) ≤ 10 mmHg, intracranial pressure (ICP) > 20 mmHg, cerebral perfusion pressure (CPP) ≤ 70 mmHg) and outcome after severe aneurysmal subarachnoid hemorrhage (SAH). In a prospective study on 42 patients monitoring of ICP, CPP, and PtiO2 (in the area at risk for vasospasm) was performed. All patients were primarily classified as Hunt and Hess grade 4 or with secondary deterioration to this grade. Relative proportions of PtiO2 ≤ 10 mmHg (n = 42), ICP > 20 mmHg (n = 25) and CPP ≤ 70 mmHg (n = 23) were derived from multimodal neuromonitoring data sets for different time intervals, i.e. 1. the total monitoring time; 2. the total monitoring time without the last two monitoring days; 3. the second last monitoring day; and 4. the last monitoring day. Patients were divided into nonsurvivors (GOS = 1) and survivors (GOS = 3-5). For the total monitoring time, significant differences in the relative proportion of critical values were found for all neuromonitoring parameters (p < 0.05). The detailed analysis of consecutive time intervals revealed significantly increased proportions of critical values in nonsurvivors for all neuromonitoring parameters during the last day only. Additionally, ICP > 20 mmHg was significantly more frequent during the second last day (p < 0.01). For other time periods no differences were observed. We conclude, that critical neuromonitoring values are not early predictors of nonsurvival in patients suffering from severe SAH.

Improvement of brain tissue oxygen and intracranial pressure during and after surgical decompression for diffuse brain oedema and space occupying infarction

BACKGROUND We evaluated the perioperative and intraoperative changes of intracranial pressure (ICP) and partial pressure of brain tissue oxygen (PtiO2) after decompressive craniectomy in patients with diffuse brain oedema and space occupying infarction. METHODS Ten patients suffering from medically intractable raised intracranial pressure (ICP) were included. The underlying diseases and causes for elevated ICP were diffuse brain oedema after subarachnoid haemorrhage (n = 3) and head injury (n = 3), or space occupying infarction of the middle cerebral artery territory due to vasospasm after SAH (n = 4). Continuous perioperative and intraoperative monitoring of PtiO2 and ICP was performed at the side of decompression. FINDINGS ICP and PtiO2 improved significantly in a uniform pattern during bone flap removal and dura opening, irrespective of the underlying disease (mean ICP from 52 mmHg to 8 mmHg, mean PtiO2 from 9 mmHg to 25 mmHg). ICP, PtiO2, and cerebral perfusion pressure were further improved in the subsequent 12 hours after surgery, as compared to the preoperative 12 hours. CONCLUSIONS Decompressive craniectomy seems to be a successful option in the treatment of intractable intracranial hypertension with associated cerebral hypoxia. These positive effects may last for several hours after the procedure irrespective of the underlying disease.

Value of Overnight Monitoring of Intracranial Pressure in Hydrocephalic Children

Objective: Exaggerated nocturnal intracranial pressure (ICP) dynamics are commonly observed in hydrocephalic children with a compromise of CSF compensatory reserve capacity. Successful shunting restores this cerebrospinal reserve. We used ICP overnight monitoring combined with positional maneuvers in complex hydrocephalic children with a suspected shunt malfunction for the assessment of shunt function. Methods: In 32 hydrocephalic children, we performed 65 computerized overnight recordings and 25 positional maneuvers. Baseline ICP was considered abnormal if it exceeded the operating pressure of the shunt by more than 2.5 mm Hg. The maximum ICP (normal = <25 mm Hg), RAP coefficient (the correlation coefficient between pulse amplitude and mean intracranial pressure, which indicates pressure volume compensatory reserve; normal = <0.6), magnitude of slow waves (SLOW) and ICP pulse amplitude (AMP) were calculated for each night. Results: Using baseline ICP, maximum ICP and RAP, 19 recordings were classified as ‘normal’ (group 1), 13 as ‘questionable’ (group 2), and 33 as ‘pathological’ (group 3) indicating shunt dysfunction or active hydrocephalus. ICP, AMP, RAP and SLOW were significantly different between groups and significantly elevated in group 3 compared to group 1. Positional tests identified shunt overdrainage in 5 of 25 occasions. In patients of group 1, who underwent revision, shunts turned out to be functional. All patients of group 3 eventually underwent shunt revision with improvement of symptoms thereafter. Conclusion: Computerized ICP monitoring can benefit the assessment of shunt function, and can accurately characterize the status of CSF compensation in shunted children with a complex presentation.

Is postoperative intensive care unit admission a prerequisite for elective craniotomy

OBJECT Routine postoperative admission to the intensive care unit (ICU) is often considered a necessity in the treatment of patients following elective craniotomy but may strain already limited resources and is of unproven benefit. In this study the authors investigated whether routine postoperative admission to a regular stepdown ward is a safe alternative. METHODS Three hundred ninety-four consecutive patients who had undergone elective craniotomy over 54 months at a single institution were retrospectively analyzed. Indications for craniotomy included tumor (257 patients) and transsphenoidal (63 patients), vascular (31 patients), ventriculostomy (22 patients), developmental (13 patients), and base of skull conditions (8 patients). Recorded data included age, operation, reason for ICU admission, medical emergency team (MET) calls, in-hospital mortality, and postoperative duration of stay. RESULTS Three hundred forty-three patients were admitted to the regular ward after elective craniotomy, whereas there were 43 planned and 8 unplanned ICU admissions. The most common reasons for planned ICU admissions were anticipated lengthy operations (42%) and anesthetic risks (40%); causes for unplanned ICU admissions were mainly unexpected slow neurological recovery and extensive intraoperative blood loss. Of the 343 regular ward admissions, 10 (3%) required a MET call; only 3 of these MET calls occurred within the first 48 postoperative hours and did not lead to an ICU admission. The overall mortality rate in the investigated cohort was 1%, with no fatalities in patients admitted to the normal ward postoperatively. CONCLUSIONS Routine ward admission for patients undergoing elective craniotomies with selective ICU admission appears safe; however, approximately 2% of patients may require a direct postoperative unplanned ICU admission. Patients with anticipated long operation times, extensive blood loss, and high anesthetic risks should be selected for postoperative ICU admission, but further study is needed to determine the preoperative factors that can aid in identifying and caring for these groups of patients.

Brain tissue oxygen (PtiO2): a clinical comparison of two monitoring devices

BACKGROUND We investigated the difference between two commercially available sensors for continuous monitoring of brain tissue oxygen (PtiO2). One is a single parameter probe for PtiO2 monitoring (Licox), the other is a multiparamter sensor (Neurotrend) further including measurement of brain temperature, pH, and partial pressure of tissue carbon dioxide. METHODS In seven patients after subarachnoid hemorrhage or traumatic brain injury continuous monitoring of PtiO2 was performed simultaneously using Licox and Neurotrend. FINDINGS Mean PtiO2 was generally lower when assessed by the Neurotrend, as compared with the Licox (Licox 27.7 mmHg vs. Neurotrend 20.9 mmHg; P = 0.028). The amplitude of PtiO2 elevations during ventilation with 100% oxygen was higher with the Licox, but this did not reach statistical significance (Licox 55.2 mmHg vs. Neurotrend 50.2 mmHg, P = 0.082). Regarding clinical stability of the sensors, only one Neurotrend sensor provided valid function over the desired monitoring period. Five Neurotrend sensors dislocated or broke and one sensor did not show any function after insertion. No malfunction occurred with the Licox sensors. CONCLUSIONS Our results suggest that PtiO2 might be lower when assessed by the Neurotrend sensor. The clinical stability of the Neurotrend sensor was of concern and allowed monitoring in one of seven patients over the desired monitoring period of several days only.